There has been a general lack of information regarding the electrophysiological consequences in activity deprived CNS neurons in mature animals due to injury, disease, aging and other factors. Little is known about the cellular property changes in cochlear nucleus neurons associated with hearing loss. Disease and age-related hearing loss is a prevalent problem especially among the aging population. Cochlear implant research has focused on how to engineer artificial devices that best simulate the coding of auditory nerve responses to sound stimuli with the assumption that hearing impaired patients have normal cochlear neuronal function that will faithfully transmit information to higher auditory centers. Recently it has been shown that bushy cells in cochlear ablated rats have elevated resting membrane potential and decreased action potential height and afterhyperpolarization, we hypothesize that these physiological property changes of AVCN bushy cells, the direct targets of auditory nerve fibers, are partly due to the change of the low- threshold potassium current and a yet to be characterized K(Ca) conductance. We further hypothesize that changes in gene expression of the excitatory synaptic receptor subunits (GluR1-4) in bushy cells are also the result of denervation due to hearing loss. We will employ a variety of electrophysiology recording techniques and quantitative RT PCR methods to test our hypotheses. These studies should shed light on the molecular basis of physiological consequences in activity deprived cochlear nucleus neurons.